Key result
Septic shock was associated with significantly lower NEP 24.11 activity compared to severe sepsis (0.10 vs. 0.50 nmole/mL/min, p<0.0001) and cardiogenic shock (0.10 vs. 0.58 nmole/mL/min, p=0.002).
Why the study?
Does baseline BNP predict fluid responsiveness and is BNP clearance altered in septic shock?
Observational (n=23)
Does baseline BNP predict fluid responsiveness and is BNP clearance altered in septic shock?
Absolute Event Rate: 0.1% vs 0.5%
p-value: p=<0.0001
High BNP levels in septic shock may be driven by impaired clearance via reduced NEP 24.11 activity, and baseline BNP does not predict fluid responsiveness in this population.
Elevated BNP may not predict fluid nonresponsiveness in septic shock; leaves open NEP's role in impaired clearance.
INTRODUCTION: High B-type natriuretic peptide (BNP) levels are reported in the context of septic shock. We hypothesized that high BNP levels might be related to an alteration in BNP clearance pathway, namely neutral endopeptidase (NEP) 24.11. NEP 24.11 activity was measured in septic shock and in cardiogenic shock patients. We further evaluated whether baseline plasma BNP can predict fluid responsiveness and whether BNP can still be released in plasma despite high initial BNP levels, in response to overloading. MATERIAL AND METHODS: Prospective observational study. Patients in severe sepsis (S) or in septic shock (SS) needing a fluid challenge were included. Stroke volume (SV) and BNP were measured before (SV1, BNP1) and 45 mins after (SV2, BNP2) a standardized fluid challenge. DeltaBNP was defined as the difference between BNP2 and BNP1. NEP 24.11 activity was determined by fluorometry in 12 SS and 4 S patients before fluid challenge and in 5 cardiogenic shock patients. RESULTS: Twenty-three patients (61 +/- 18 years old, Simplified Acute Physiology Score II: 54 +/- 21; 19 SS, 4 S; BNP1: 1371 +/- 1434 pg/mL) were studied. BNP1 concentrations were significantly higher in SS than in S (1643 +/- 1437 vs. 80 +/- 35 pg/mL; p = 0.002). There was no correlation between baseline BNP and fluid responsiveness. Nine of the 11 patients with BNP1 >1000 pg/mL were fluid responders. DeltaBNP was greater in fluid nonresponders than in fluid responders (22 +/- 27% vs. 6 +/- 11%, p = 0.028). Plasma BNP was higher in SS than in cardiogenic shock patients (1367 +/- 1438 vs. 750 +/- 346 respectively; p = 0.027). NEP 24.11 activity was lower in SS than in S patients (0.10 +/- 0.06 nmole/mL/min vs. 0.50 +/- 0.22 nmole/mL/min, p <0.0001) cardiogenic shock patients (0.10 +/- 0.06 nmole/mL/min vs. 0.58 +/- 0.19 nmole/mL/min; p = 0.002). CONCLUSION: High levels of BNP might be related to an alteration in BNP clearance. During sepsis, high BNP levels are not predictive of fluid nonresponsiveness. Nevertheless, in fluid nonresponders, acute ventricular stretching can result in further BNP release.
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Pirracchio et al. (2008) conducted an observational in Severe sepsis and septic shock (n=23). Septic shock vs. Severe sepsis was evaluated on NEP 24.11 activity (nmole/mL/min) (p=<0.0001). Septic shock was associated with significantly lower NEP 24.11 activity compared to severe sepsis (0.10 vs. 0.50 nmole/mL/min, p<0.0001) and cardiogenic shock (0.10 vs. 0.58 nmole/mL/min, p=0.002).
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